Group B Streptococci (GBS) are a major cause of morbidity and mortality in neonates and in other patients with compromised host defense mechanisms. The importance of GBS disease for newborn infants in the United States was underscored in an NIH sponsored workshop on Group B Streptococcal Infection. Fisher, G. S. (1983) J. Infect. Dis. 148, 163-166.
The incidence of GBS disease is estimated at between 2 to 5 cases per 1000 live births. Pass, M.A. (1979) J. Pediatr. 795, 437-443. At highest risk are premature infants, whose birth weight is less than 2500 grams and infants born to mothers with premature rupture of membranes. Fisher, G. W., supra. Susceptibility to and severity of GBS disease has been associated with several risk factors including deficient or altered host defense mechanisms. Hill, H. R. et al. (1979) Pediatrics 64, 5787-5794. Studies have shown that human neonates who develop Group B Streptococcal Sepsis usually lack opsonic antibody to their infecting strain. Opsonic antibody is antibody that combines with antigen and facilitates ingestion of the antigen by phagocytes. In addition, these neonates usually have impaired polymorphonuclear leukocyte (PMN) function. Hemming, V. G. et al. (1976) J. Clin. Invest. 58, 1379-1387; Shigeoka, A. S. et al. (1979) J. Pediatr. 95, 454-460.
Despite aggressive supportive therapy and early institution of appropriate antimicrobial agents, the mortality rate for early-onset Group B Streptococcal Disease continues to be in the 25-75% range. This observation has prompted considerable interest and research in the development and use of adjunctive treatment modalities, which focus on improving the host's immune status, including a vaccine for maternal immunization [Baker, C. J. et al. (1978) J. Clin. Invest. 61, 1107-1110]; the use of ante and intrapartum prophylactic antibiotics; and various blood components including: whole blood, polymorphonuclear leukocytes, and immune serum globulins modified for intravenous use. However, despite such investigative work with animal models of disease, the mechanisms of host resistance to GBS have not been clearly defined. Some strains of GBS appear to be more virulent than others. Furthermore, all GBS strains are not uniformly susceptible to the action of antibody and complement.
Susceptibility to GBS disease, like to other infectious diseases, is multi-factorial and impinges on native and acquired immunity which are influenced by the host's genetic constitution, sex, age, and nutritional status. Of the aforementioned factors, there is very little information available as to the role of single or aggregate nutrients on host resistance to GBS disease. Almost any nutritional deficiency or excess may affect adversely one or more components of the immune system. Conversely the same nutrients that impinge on the immune system may also be essential for the multiplication and virulence of certain pathogenic microorganisms.
The need for a safe and effective regimen for preventing GBS infection in newborns was made evident in a recent editiorial, "Prevention of Early-Onset Group B Streptococcal Infection in the Newborn" (1984) Lancet 1, 1056-1058. In evaluating one potential regimen, antibiotic prophylaxis, the author concluded that firm recommendations as to its use must await further experimentation.